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Opn4m2 (show OPN4 Proteins) labeling shows nuclear localization, which did not change in response to light. opn4m1 (show OPN4 Proteins), opn4m2 (show OPN4 Proteins), gr, per1b, and cry1b presented an oscillatory profile of expression in LD condition. In both DD and LD condition, dexamethasone (DEX) treatment shifted the peak expression of per1b and cry1b transcripts
Data (including data from studies in knockout/transgenic mice) suggest that, under hypoxic conditions, muscle atrophy and elevated gene expression of ubiquitin proteasomal system-associated enzymes are mostly independent of glucocorticoid/Nr3c1 signaling.
We propose that the GC-induced mitochondrial accumulation of Bax (show BAX Proteins) and the interaction between the GR and Bim (show BCL2L11 Proteins), Bcl-xL (show BCL2L1 Proteins) and Bak (show BAK1 Proteins) could play a role in the regulation of thymocyte apoptosis.
The potentiation of RANKL (show TNFSF11 Proteins) induced CTX release by dexamethasone was significantly less in bone marrow macrophage cells from mice with conditional knockout of the osteoclastic glucocorticoid receptor and completely absent in cells from GR(dim) mice, which carry a point mutation in one dimerizing interface of the GC receptor.
These data establish SUMO conjugation as a novel regulatory mechanism in the Hsp90 (show HSP90 Proteins) cochaperone activity of FKBP51 (show FKBP5 Proteins) with a functional impact on GR signaling in a neuronal context.
These results together suggested that ERK1 (show MAPK3 Proteins) phosphorylation plays a critical role in regulating GR beta expression and hydrocortisone-induce GR phosphorylation at Ser220, which is critical for the anti-apoptotic effects hydrocortisone on hepatic ischemia-reperfusion injury.
a significant protein-protein interaction between GR and CHOP (show DDIT3 Proteins), (GR-CHOP (show DDIT3 Proteins) heterocomplex formation) under endoplasmic reticulum stress conditions, is reported.
This study identifies an endocrine developmental axis in which fetal GR primes the activity of PPARalpha (show PPARA Proteins) in anticipation of the sudden shifts in postnatal nutrient source and metabolic demands.
Skin differentiation is impaired, and both apoptosis and cell proliferation are augmented in the absence of p23 (show CDK5R1 Proteins); the consequences are a severe thinning of the stratum corneum and reduced numbers of hair follicles. Since the phenotype of p23 (show CDK5R1 Proteins)-null embryos is strikingly similar to that of embryos lacking the glucocorticoid receptor, a paradigmatic Hsp90 (show HSP90 Proteins)-p23 (show CDK5R1 Proteins) client protein, we investigated glucocorticoid signaling.
REV-ERBalpha (show NR1D1 Proteins) binds to the C-terminal portion and GR to the N-terminal portion of HSP90alpha (show HSP90AA2 Proteins) and HSP90beta (show HSP90AB1 Proteins), a chaperone responsible for the activation of proteins to ensure survival of a cell.
Phospho-AMPK (show PRKAA1 Proteins) is a molecular switch able to cooperate with glucocorticoid receptors and Ppar-alpha (show PPARA Proteins) at the chromatin level, a novel adaptation mechanism to prolonged fasting.
The guinea pig GR-specific mutations within the H1-H3 loop confer global changes within the GR-Hsp90 (show HSP90 Proteins) complex that favor FKBP51 (show FKBP5 Proteins) repression over FKBP52 (show FKBP4 Proteins) potentiation.
This review focuses on the earlier findings on the pathophysiology of GR signaling and presents criteria facilitating identification of novel NR3C1 mutations in selected patients. [review]
The BclI NR3C1 polymorphisms were significantly associated with asthma in adults. (Meta-analysis)
Here we show genome-wide that blocked GBR generally require CHD9 and BRM (show SMARCA2 Proteins) for GR occupancy in contrast to GBR that are not blocked by Hic-5 (show TGFB1I1 Proteins). Hic-5 (show TGFB1I1 Proteins) blocked GBR are enriched near Hic-5 (show TGFB1I1 Proteins) blocked GR target genes but not near GR target genes that are not blocked by Hic-5 (show TGFB1I1 Proteins).
There was no significant association between different genotypes and alleles of Glucocorticoid Receptor of rs6195, rs6189/rs6190 variants, and response to fluoxetine (p=0.213 and 0.99, respectively).
NR3C1 gene polymorphisms are significantly associated with the response to glucocorticoids.
There is no clear evidence that the analysed NR3C1 allelic variants confer a risk for developing systemic autoimmune diseases although the minor G allele of rs41423247 may be protective among Caucasians (review and meta-analysis).
Analyses demonstrated a trend in the association between maternal trait anxiety and depression symptoms with placental gene expression of NR3C1. We found a significant interaction with maternal ethnicity. In Caucasians only, prenatal trait anxiety and depressive symptoms were associated with an increase in placental NR3C1 expression, and prenatal life events were associated with a down regulation of HSD11B2 (show HSD11B2 Proteins)
We genotyped 10 single nucleotide polymorphisms (SNPs) on the NR3C1 gene (rs10482682, rs33389, rs10482633, rs10515522, rs2963156, rs4128428, rs9324918, rs41423247, rs6189, rs10052957).Haplotype analyses revealed significant effects of NR3C1 (p = 0.011) on cortisol stress response. Neither NR3C1 haplotype nor NR3C2 (show NR3C2 Proteins) haplotype was associated with reasoning abilities.
In this study, we described the cellular localization of the glucocorticoid receptor in the human adult and fetal testis and provided evidence of an association between semen quality and a genetic polymorphism BclI (rs41423247) in the NR3C1 gene.
Results indicate that maltreated children evidence higher baseline levels of NR3C1 methylation, significant decreases in methylation over time, and then at follow-up, lower levels of methylation, relative to nonmaltreated preschoolers.
This study reveals the role of GR in muscle fiber inhibition on intramuscular adipocytes, and identifies myostatin (show MSTN Proteins) as a muscle-derived modulator for adipose GR level.
These results indicate that myostatin (show MSTN Proteins) mediates maternal low protein diet-induced growth retardation, through epigenetic regulation involving FoxO3 (show FOXO3 Proteins) and glucocorticoid receptor binding to its promoter.
Data indicate that higher hepatic glucocorticoid receptor (GR) expression in EHL piglets attributes mainly to the enhanced transcription of GR promoter 1-9/10 from breed-specific interaction of p53 (show TP53 Proteins) and specificity protein 1 (Sp1 (show SP1 Proteins)).
Tissue specificities, gene expression and induction responsiveness of the porcine NR3C1 gene.
Cloning and dna sequence analysis of the upstream flanking region of the NR3C1 gene in the domestic pig.
Effects of age, weaning and/or social isolation on the expression of genes regulating glucocorticoid response [glucocorticoid receptor).
Glucocorticoid Receptor protein expression in granulosa cells was higher in cysts from animals with spontaneous cystic ovarian disease and adrenocorticotropic hormone-induced cystic ovarian disease than in tertiary follicles from control animals.
Exposure to follicular fluid transiently increased the transcript levels of IL8 (show IL8 Proteins) and PTGS2 (show PTGS2 Proteins), and decreased the expression of SOD2 (show SOD2 Proteins), GPX3 (show GPX3 Proteins), DAB2 (show DAB2 Proteins), and NR3C1. TNF (show TNF Proteins) and IL6 (show IL6 Proteins) levels were also decreased while those of NAMPT (show NAMPT Proteins) were unaffected.
Bayesian image analysis of dexamethasone and shear stress-induced glucocorticoid receptor intracellular movement
investigation of gene expression for GR, 11HSD1, and 11HSD2 (show HSD11B2 Proteins) in granulosa cells and theca interna layers during follicular maturation and atresia: expression of GR was largely unchanged during follicular maturation
The E domain of the trout receptors are not involved in the nucleocytoplasmic localization of naive trout GRs (show GARS Proteins), but the A/B domain, especially if linked to the corresponding trout CD region, plays a pivotal role in the cellular distribution pattern.
This gene encodes glucocorticoid receptor, which can function both as a transcription factor that binds to glucocorticoid response elements in the promoters of glucocorticoid responsive genes to activate their transcription, and as a regulator of other transcription factors. This receptor is typically found in the cytoplasm, but upon ligand binding, is transported into the nucleus. It is involved in inflammatory responses, cellular proliferation, and differentiation in target tissues. Mutations in this gene are associated with generalized glucocorticoid resistance. Alternative splicing of this gene results in transcript variants encoding either the same or different isoforms. Additional isoforms resulting from the use of alternate in-frame translation initiation sites have also been described, and shown to be functional, displaying diverse cytoplasm-to-nucleus trafficking patterns and distinct transcriptional activities (PMID:15866175).
, nuclear receptor subfamily 3, group C, member 1
, glucocorticoid receptor 1
, nuclear receptor subfamily 3 group C member 1
, glucocorticoid nuclear receptor variant 1
, glucocorticoid receptor alpha
, glucocorticoid receptor variant P
, glucocorticoid receptor variant beta
, glucocorticoid receptor variant gamma